W Zhou et al.
The Journal of clinical investigation, 105(10), 1363-1371 (2000-05-17)
Previous work has indicated that complement is a mediator of ischemia/reperfusion (I/R) injury. To investigate the components of complement responsible for this effect, we examined a model of renal I/R injury in C3-, C4-, C5-, and C6-deficient mice. We occluded